Is Parkinson’s Disease Hereditary? What to Know About Genetic Risk

Is Parkinson’s Disease Hereditary?

Family history plays a role in a small percentage of cases, but environmental factors and age also heighten the risk.
mature woman's hand leafing through old family photo album
Some people with Parkinson’s have a family history, and some genetic features are more common in such families.Getty Images
Parkinson’s disease can be due to genetic or environmental factors. It can be familial, meaning it runs in families, or idiopathic, when there’s no clear cause. Most cases of Parkinson’s disease are idiopathic and appear after age 60.

However, 10 to 15 percent of cases occur in people with a family history. Familial Parkinson’s can appear earlier, with symptoms starting between age 21 and 50. Less commonly, juvenile Parkinson’s disease appears before age 21. Around 20 to 30 percent of people with early-onset Parkinson’s have a family history, compared with 10 to 15 percent of those with late-onset disease.

Changes in various genes may increase the risk of Parkinson’s to different extents, but having a genetic mutation does not mean you will develop or pass on Parkinson’s.

In this article, we look at the role of genetic factors in Parkinson’s disease.

How Family History and Risk Factors Relate to Parkinson’s Disease

Parkinson’s disease is a progressive condition that affects the brain. It leads to tremors, rigidity, and other movement problems. Eventually, it can cause dementia.

Symptoms result from the destruction of certain nerve cells and the buildup of proteins known as Lewy bodies in the brain.

The most likely causes of Parkinson’s disease are genetic, epigenetic, and environmental.

Genetic Causes

Having Parkinson’s-related genetic features doesn’t always mean you’ll get Parkinson’s disease.

Depending on the gene, effects can vary:

  • Causing or significantly increasing the risk of Parkinson’s
  • Increasing the risk but to a lesser extent
  • Increasing the risk but only in certain circumstances

Some genes are specific to familial and early-onset Parkinson’s disease, while others are present with either idiopathic Parkinson’s, or both familial and early-onset Parkinson's.

Scientists have linked changes in 90 genes to Parkinson’s, and they are still finding more.

Genetic findings help us understand many aspects of the disease:

  • How people inherit Parkinson’s
  • How it develops
  • Who’s likely to get it
These findings may also help identify ways to cure or prevent Parkinson’s disease.

It is also important to note that there are two types of inheritence.

Direct inheritance occurs when genetic features that pass from parents to children lead directly to Parkinson’s. The SNCA, LRRK2, PARK7, PINK1, and PRKN genes can do this.


Indirect inheritence occurs when the changes to genes don’t necessarily always lead to Parkinson’s. Inheriting a single mutation in the GBA1 gene (meaning you are a carrier) increases your risk of Parkinson's disease by 20 to 30 times. If you have a GBA1 mutation, there is about a 30 percent chance that you’ll have the neurologic effects of Parkinson’s Overall, GBA1 is the most important and common genetic risk factor for Parkinson’s.


Epigenetic Changes

Not all genetic changes are inherited. Exposure to toxins or other triggers can change a gene. Your genetic DNA sequence is inherited and always stays the same. Epigenetic changes affect which genes are active. This affects the way your body makes proteins, with important implications for your health.

Some experts believe that epigenetic changes contribute to Parkinson’s. This could result, for instance, from exposure to environmental toxins such as pesticides.


Environmental Factors

Environmental factors may trigger epigenetic changes or cause Parkinson’s to develop in those with certain inherited genetic factors.

According to the Parkinson’s Foundation, risk factors include exposure to these items:


  • Pesticides
  • Herbicides
  • Substances used in chemical warfare such as Agent Orange
  • Repeated head trauma, as happens in contact sports
  • Solvents such as trichloroethylene
  • Polychlorinated biphenyls
The authors of a research article published in 2024 argue that toxins that damage mitochondria, the powerhouse of a cell, are the most likely environmental cause of Parkinson’s. Living near an industrial site or in an area with high levels of air pollution may increase your risk.

Genes Linked to Parkinson’s Disease

Here are some of the main genes linked to Parkinson’s, including some that may be inherited. Changes in all of these genes are relatively rare.


SNCA

SNCA was the first gene that scientists associated with Parkinson’s disease. In 1997, researchers found SNCA changes in several families with a history of Parkinson’s.

SNCA is linked with early-onset Parkinson’s. This is when symptoms appear before age 50.

SNCA tells the body to make alpha-synuclein, a protein that likely performs several functions in nerve cells but can also form clumps called Lewy bodies in the brains of people with Parkinson’s.

SNCA changes are a strong predictor of Parkinson’s disease.

LRRK2

Changes in the LRRK2 gene account for 1 to 2 percent of all cases of Parkinson’s. LRRK2 tells the body to produce the LRRK2 protein.

Too much activity in this protein increases the risk of Parkinson’s disease.

 It causes a buildup of waste cell material, leading to higher levels of reactive oxygen species, lower levels of adenosine triphosphate, and other damaging changes.

Changes in LRRK2 are common with familial Parkinson’s disease but can also occur without a family history. Symptoms develop around the same age in both cases.

LRRK2 is more often linked to Parkinson’s in people of Ashkenazi (Eastern European) Jewish and North African Berber descent.

LRRK2 changes significantly increase your risk of Parkinson’s disease.

PARK2

PARK2 tells the body to make the protein parkin. Parkin helps the body break down unwanted cell material and recycle proteins.

Changes in PARK2 increase the risk of young-onset Parkinson’s disease. This often appears when people are in their twenties or thirties, but it can emerge in children as young as 10.


PARK7

Changes in PARK7 can lead to a rare type of early-onset Parkinson’s disease that progresses slowly and involves the development of Lewy bodies.

The PARK7 protein prevents damage to other proteins and metabolites (substances that break down waste in the body). Low PARK7 activity can result in a buildup of waste and cell damage that might lead to Parkinson’s.

PINK1

The PINK1 gene instructs the body to make a protein kinase (an enzyme) that protects the insides of cells from stress.

Changes in this gene are linked to familial Parkinson’s and can lead to early-onset disease.


GBA1

Experts have linked Parkinson’s with low activity in the glucocerebrosidase beta (GBA1) gene, which tells the body to make the glucocerebrosidase protein. A GBA1 mutation is the most common genetic change in people with Parkinson’s, present in 5 to 15 percent of those with the disease.

GBA1 changes can occur in people with either familial or idiopathic Parkinson’s disease. In GBA1-associated familial disease, the symptoms tend to start earlier than for idiopathic, the effect on thinking is more severe, and the disease progresses more rapidly. Changes in GBA1 are most common in people of Ashkenazi Jewish descent.


Will I Get Parkinson’s If I Test Positive for These Gene Changes?

We asked Rebecca Gilbert, MD, PhD, from the American Parkinson Disease Association, about the likelihood of developing Parkinson’s if you test positive for changes in Parkinson's-associated genes.

Dr. Gilbert is a neurologist, movement disorders specialist, and practicing physician who diagnoses and treats people with Parkinson’s disease. She says, “Testing positive for one of these genes doesn’t necessarily mean you’ll develop Parkinson’s disease.”

She explains that each gene affects your risk differently. For instance, you need only one faulty LRRK2 gene to develop Parkinson’s. However, only around 30 percent of people with LRRK2 changes will get Parkinson’s.

Should I Get Genetic Testing for Parkinson’s Disease?

If you have a family history of Parkinson’s disease, you may wonder about testing for the genetic features that increase your risk.

However, it’s worth remembering a few points:


  • Only 10 to 15 percent of Parkinson’s is familial.
  • Genetic factors are not the only cause of Parkinson’s.
  • Testing positive for a genetic feature doesn’t mean you will develop symptoms and could lead to unnecessary anxiety.

Gilbert notes that tests for Parkinson’s cover up to 44 genes. Such a wide range can be confusing, and it’s not always clear which genetic changes will affect an individual or how.

She adds that how individuals feel about testing for their risk of developing Parkinson’s varies: “Some may want to know everything they can about their health. Others may feel that if there are no clinical trials to participate in and no preventive medications to take to reduce their future risk of developing Parksinson’s, they don’t want to know whether they harbor a mutation.”

While exercise is good for everyone’s health, Gilbert points out that it may modify your risk of developing Parkinson’s. So if tests suggest that you have higher risk of Parkinson’s, exercise may be a positive lifestyle change. It’s essential to discuss these issues with a genetic counselor before and after testing.


If I Have Parkinson’s Disease, Will My Children Develop It?

Some people with Parkinson’s have a family history, and some genetic features are more common in such families.

Most people with Parkinson’s don’t have a known family history, but inherited changes on the SNCA, LRRK2, PARK7, PINK1, and PRKN genes can directly increase the risk.

If you inherit changes in the LRRK2 or SNCA genes, you need only one copy of the affected gene to have Parkinson’s.

Most of those people have one parent with the condition. Even then, only around 30 percent of these people develop the disease.

If you have changes on the PARK7, PINK1, or PRKN genes, you’ll get Parkinson’s only if you have two copies of mutated genes. In this case, both your parents will have one copy, but they most likely did not have symptoms.

Gilbert notes, “Genetic testing of people who have a family history of Parkinson’s disease but do not have symptoms is tricky. Most people with Parkinson’s do not harbor one of the known genetic mutations associated with the disease. Therefore, if that person’s child is tested, the most likely scenario is that no mutation will be identified. But that does not mean that the child does not have an increased risk of Parkinson’s. It just means that the genetic contribution to that person’s Parkinson’s risk is not known.”

She adds that many people with an abnormal gene will never develop Parkinson’s.

The Takeaway

  • Having a family history of Parkinson’s disease doesn’t mean you will develop it, although it does increase your chances.
  • Genetic, epigenetic, and environmental factors all contribute to the onset of the disease.
  • If family members have Parkinson’s diagnosis, you can take genetic tests to find out your risk. However, it’s best to speak with a doctor or counselor first as the results are often not conclusive.

Resources We Trust

jason-paul-chua-bio

Jason Paul Chua, MD, PhD

Medical Reviewer

Jason Chua, MD, PhD, is an assistant professor in the Department of Neurology and Division of Movement Disorders at Johns Hopkins School of Medicine. He received his training at the University of Michigan, where he obtained medical and graduate degrees, then completed a residency in neurology and a combined clinical/research fellowship in movement disorders and neurodegeneration.

Dr. Chua’s primary research interests are in neurodegenerative disease, with a special focus on the cellular housekeeping pathway of autophagy and its impact on disease development in diseases such as Parkinson disease. His work has been supported by multiple research training and career development grants from the National Institute of Neurological Disorders and Stroke and the American Academy of Neurology. He is the primary or coauthor of 14 peer-reviewed scientific publications and two peer-reviewed online learning modules from the American Academy of Neurology. He is also a contributing author to The Little Black Book of Neurology by Osama Zaldat, MD and Alan Lerner, MD, and has peer reviewed for the scientific journals Autophagy, eLife, and Neurobiology of Disease.

Yvette Brazier

Author

Yvette Brazier's career has focused on language, communication, and content production, particularly in health education and information. From 2005 to 2015, she supported learning in the health science department of a higher education establishment, teaching the language of health, research, and other language application skills to paramedic, pharmacy, and medical imaging students.

From 2015 to 2023, Yvette worked as a health information editor at Medical News Today and Healthline. Yvette is now a freelance writer and editor, preparing content for Everyday Health, Medical News Today, and other health information providers.

EDITORIAL SOURCES
Everyday Health follows strict sourcing guidelines to ensure the accuracy of its content, outlined in our editorial policy. We use only trustworthy sources, including peer-reviewed studies, board-certified medical experts, patients with lived experience, and information from top institutions.
Resources
  1. Zafar S et al. Parkinson Disease. StatPearls. August 2023.
  2. Kolicheski A et al. Early-Onset Parkinson’s Disease: Creating the Right Environment for a Genetic Disorder. Journal of Parkinson’s Disease. December 2022.
  3. Genetics and Parkinsons. Parkinson’s Foundation.
  4. Parkinson’s Disease. National Institute of Neurologial Disorders and Stroke. September 2024.
  5. Song H et al. Epigenetic Modification in Parkinson’s Disease. Frontiers in Cell and Developmental Biology. June 2023.
  6. Bandres-Ciga S et al. Genetics of Parkinson's disease: An introspection of its journey towards precision medicine. Neurobiology of Disease. April 2020.
  7. Parkinson’s Disease. MedlinePlus. May 2012.
  8. Migdalska-Richards A et al. The relationship between glucocerebrosidase mutations and Parkinson disease. Journal of Neurochemistry. February 2016.
  9. Epigenetics, Health, and Disease. Centers for Disease Control and Prevention. May 2024.
  10. Klokkaris A et al. An Overview of Epigenetic Changes in the Parkinson’s Disease Brain. International Journal of Molecular Sciences. June 2024.
  11. Environmental Factors. Parkinson’s Foundation.
  12. Dorsey ER et al. Parkinson’s Disease Is Predominantly an Environmental Disease. Journal of Parkinson’s Disease. April 2024.
  13. Parkinson’s Genetics. Michael J. Fox Foundation for Parkinson's Research.
  14. The Genetic Link to Parkinson's Disease. Johns Hopkins Medicine.
  15. Zilocchi M et al. Exploring the Impact of PARK2 Mutations on the Total and Mitochondrial Proteome of Human Skin Fibroblasts. Frontiers in Cell and Developmental Biology. June 2020.
  16. Taymans JM et al. Perspective on the current state of the LRRK2 field. Nature: NPJ Parkinson’s Disease. July 2023.
  17. Mizuno Y. More Than 20 Years of the Discovery of Park2. Neuroscience Research. October 2020.
  18. Heremans IP et al. Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite. Proceedings of the National Academy of Sciences of the United States of America. January 2022.
  19. Quinn PMG et al. PINK1/PARKIN signalling in neurodegeneration and neuroinflammation. Acta Neuropathologica Communications. November 2020.
  20. Smith L et al. GBA Variants and Parkinson Disease: Mechanisms and Treatments. Cells. April 2022.
  21. Genetic Testing and Counseling. Parkinson’s Foundation.
  22. Trinh J et al. Disease penetrance of late-onset parkinsonism: A meta-analysis. JAMA Neurology. December 2014.
  23. Saunders-Pullman R et al. LRRK2 Parkinson Disease. Gene Reviews. November 2006.